Suspected malnutrition-induced reversible feline skin fragility syndrome in a cat with congenital axial deformities.

A stray cat, an intact female Japanese domestic shorthair cat of unknown age (suspected to be a young adult), was rescued. The cat was lethargic and thin and had marked skin fragility, delayed wound healing without skin hyperextensibility, and hind limb proprioceptive ataxia and paresis. Survey radiography, computed tomography, and magnetic resonance imaging revealed congenital vertebral anomalies, including thoracolumbar transitional vertebrae, scoliosis resulting from a thoracic lateral wedge-shaped vertebra, and a kinked tail, and a dilated spinal cord central canal. Through nutritional support, the cat's general condition normalized, followed by a gradual and complete improvement of skin features. Whole-genome sequencing was completed; however, no pathogenic genetic variant was identified that could have caused this phenotype, including congenital scoliosis. A skin biopsy obtained 7 y after the rescue revealed no remarkable findings on histopathology or transmission electron microscopy. Based on clinical course and microscopic findings, malnutrition-induced reversible feline skin fragility syndrome (FSFS) was suspected, and nutritional support was considered to have improved the skin condition. Key clinical message: This is the second reported case of presumed malnutrition-induced reversible FSFS and was accompanied by long-term follow-up.

Syndrome de fragilité cutanée réversible induit par la malnutrition soupçonné chez un chat avec des difformités axiales congénitales. Un chat errant, une femelle intacte de race japonaise à poil court et d'âge inconnu (suspecté être une jeune adulte), a été secourue. La chatte était léthargique et maigre, et avait une fragilité marquée de la peau, un retard dans la guérison de plaies sans hyperextensibilité de la peau, et une ataxie proprioceptive et parésie des membres postérieurs. Des radiographies, un examen par tomodensitométrie, et de l'imagerie par résonnance magnétique ont révélé des anomalies congénitales des vertèbres, incluant des vertèbres transitionnelles thoraco-lombaires, une scoliose résultant d'une vertèbre thoracique en forme de coin, une queue pliée, et un canal central de la moelle épinière dilaté. Grâce à un soutien nutritionnel, la condition générale du chat s'est stabilisée, suivi d'une amélioration graduelle et complète des caractéristiques de la peau. Le séquençage du génome complet a été effectué; toutefois, aucune variation génétique pathogénique n'a été identifiée qui aurait pu causer ce phénotype, incluant la scoliose congénitale. Une biopsie cutanée obtenue 7 j après le sauvetage n'a révélé aucune trouvaille spéciale à l'histopathologie ou par microscopie électronique à transmission. Basé sur le déroulement clinique et l'examen microscopique, le syndrome de fragilité cutanée réversible félin induit par la malnutrition (FSFS) était suspecté, et le soutien nutritionnel a été considéré comme ayant amélioré la condition cutanée.Message clinique clé :Ce cas est le deuxième cas rapporté de FSFS induit par la malnutrition soupçonné et a fait l'objet d'un suivi à long terme.(Traduit par Dr Serge Messier).

A de novo mutation in CACNA1A is associated with autosomal dominant bovine familial convulsions and ataxia in Angus cattle.

Bovine familial convulsions and ataxia (BFCA) is considered an autosomal dominant syndrome with incomplete penetrance. Nine Angus calves from the same herd were diagnosed with BFCA within days of birth. Necropsy revealed cerebellar and spinal cord lesions associated with the condition. Parentage testing confirmed that all affected calves had a common sire. The sire was then bred to 36 cows across two herds using artificial insemination, producing an additional 14 affected calves. The objective of this investigation was to identify hypothesized dominant genetic variation underlying the condition. Whole-genome sequencing was performed on the sire, six affected and seven unaffected paternal half-sibling calves and combined with data from 135 unrelated controls. The sire and five of the six affected calves were heterozygous for a nonsense variant (Chr7 g.12367906C>T, c.5073C>T, p.Arg1681*) in CACNA1A. The other affected calves (N = 8) were heterozygous for the variant but it was absent in the other unaffected calves (N = 7) and parents of the sire. This variant was also absent in sequence data from over 6500 other cattle obtained via public repositories and collaborator projects. The variant in CACNA1A is expressed in the cerebellum of the ataxic calves as detected in the transcriptome and was not differentially expressed compared with controls. The CACNA1A protein is part of a highly expressed cerebellar calcium voltage gated channel. The nonsense variant is proposed to cause haploinsufficiency, preventing proper transmission of neuronal signals through the channel and resulting in BFCA.

Measurement of 8-hydroxy-2'-deoxyguanosine in serum and cerebrospinal fluid of horses with neuroaxonal degeneration and other causes of proprioceptive ataxia.

BACKGROUND: Eight-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of oxidative damage evaluated in human neurodegenerative disease, has potential to correlate with postmortem diagnosis of neuroaxonal dystrophy/degenerative myeloencephalopathy (NAD/DM) in horses. HYPOTHESIS: We hypothesized that 8-OHdG will be higher in CSF and serum from NAD/DM horses compared with horses with other neurologic diseases (CVSM, EPM) and a control group of neurologically normal horses. We also hypothesized that 8-OHdG will be higher in CSF compared with serum from NAD/DM horses. ANIMALS: Fifty client-owned horses with postmortem diagnoses: 20 NAD/DM, 10 CVSM, 10 EPM, and 10 control horses. Serum and CSF samples were obtained between November 2010 and March 2022. METHODS: Case-control study using biobanked samples was performed and commercial competitive ELISA kit (Highly Sensitive 8-OHdG Check ELISA) utilized. Concentration of 8-OHdG was quantitated in both CSF and serum and compared between groups. RESULTS: No correlation was established between the measures of 8-OHdG in serum and CSF and group. CSF median [8-OHdG] for NAD/DM was 169.9 pg/mL (IQR25-75 : 67.18-210.6), CVSM 157.1 pg/mL (IQR25-75 : 132.1-229.1), EPM 131.4 pg/mL (IQR25-75 : 102.1-193.2), and control 149.8 pg/mL (IQR25-75 : 113.3-196.4). Serum median [8-OHdG] for NAD/DM was 130 pg/mL (IQR25-75 : 51.73-157.2), CVSM 125.8 pg/mL (IQR25-75 : 62.8-170.8), EPM 120.6 pg/mL (IQR25-75 : 87.23-229.7), and control 157.6 pg/mL (IQR25-75 : 97.15-245.6). Poisson regression analysis showed no difference established once confounding variables were considered. CONCLUSIONS: Eight-OHdG did not aid in antemortem diagnosis of NAD/DM in this cohort of horses. At the time of diagnosis horses with NAD/DM do not have ongoing oxidative stress.

Medial strabismus (esotropia) at rest associated with contralateral paramedian thalamic ischemic infarction in 2 dogs.

Pseudoabducens paralysis resulting in resting medial strabismus (esotropia) is a rare consequence of a contralateral paramedian thalamic ischemic infarction in people. To date, esotropia has been reported in dogs in association with ipsilateral abducens neuropathy or extraocular myopathy, but not secondary to thalamic lesions. A 7-year-old male neutered Border Collie and a 12-year-old female neutered cross-breed dog were presented with peracute nonprogressive vestibular ataxia. Neurological examination identified right esotropia, nonambulatory tetraparesis, right head tilt, vestibular ataxia and nystagmus. Lesions in both dogs were localized to the vestibular system with thalamic involvement. Magnetic resonance imaging of the brain identified a left paramedian thalamic lacunar ischemic infarct in both dogs. Interruption of descending inhibitory pathways that decussate in the subthalamic region and innervate the contralateral motor nucleus of the oculomotor nerve leads to hypertonicity of the medial rectus. These cases indicate that esotropia is a rare but highly localizing sign in dogs with contralateral thalamic infarcts.

Evaluation of pharmacological alternatives to reduce the pain and discomfort produced by electroejaculation in rams.

Electroejaculation (EE) represents the main technique for semen collection from domestic and wild animals independently of libido. However, the technique is associated with intense involuntary muscle contractions, vocalization, ataxia and lying down, caused by the electric stimulation of the nerves in the caudal epigastric region. These clinical manifestations represent important indicators of discomfort. In this context, the objective of this study was to evaluate two protocols of local anaesthetic blockade and two anatomical access for pharmacological desensitization of the caudal epigastric innervation as alternatives to promote comfort and reduce stress associated with EE in rams. For the study, four clinically healthy Dorper rams were selected. All animals were subjected to a design consisting of five semen collection treatments (n = 3 collections per treatment): T1-control, conventional EE without local anaesthetic blockade; T2, EE with ventral blockade (VB) of epigastric innervation using lidocaine hydrochloride 2%; T3, EE with VB of epigastric innervation using a combination of lidocaine hydrochloride 2% and fentanyl citrate; T4, EE with blockade of epigastric innervation through the perineal access using lidocaine hydrochloride 2%; T5, EE with blockade of epigastric innervation through the perineal access using a combination of lidocaine hydrochloride and fentanyl citrate. Seminal samples resulting from EE were subjectively evaluated for sperm motility and concentration, vigour and volume. Additionally, blood serum samples were collected for quantification of cortisol and creatine kinase (CK) enzyme. Assessments of stress and discomfort were conducted by measuring blood pressure, heart rate (HR) and respiratory rate (RR), as well as observing involuntary muscle contractions, ataxia and animal vocalization. No variations in blood pressure, sperm motility, vigour, CK, and cortisol were observed among the treatments. Individual variations were observed for the occurrence of vocalization (p = .0066), but there were no differences between the groups. Anaesthetic blockades conducted using the combination of lidocaine and fentanyl resulted in a lower incidence of ataxia during EE (p < .0001). It is concluded that the combination of fentanyl citrate and lidocaine hydrochloride results in less discomfort for animals undergoing EE, regardless of the anatomical access used for local anaesthetic blockades.

Clinical and histopathological features in horses with neuroaxonal degeneration: 100 cases (2017-2021).

BACKGROUND: Adult horses with proprioceptive ataxia and behavior changes that have histologic lesions consistent with neurodegenerative disease have been increasingly recognized. HYPOTHESIS/OBJECTIVES: Describe the history, clinical findings and histopathologic features of horses presented to a referral institution with neuroaxonal degeneration. ANIMALS: One hundred horses with a necropsy diagnosis of neuroaxonal degeneration compatible with neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM). METHODS: Retrospective study of horses presented to the University of Pennsylvania, New Bolton Center, between 2017 and 2021 with a necropsy diagnosis of eNAD/EDM. RESULTS: Affected horses had a median age of 8 years (range, 1-22), and the majority were Warmbloods (72). Sixty-eight horses had behavioral changes, and all 100 had proprioceptive ataxia (median grade, 2/5). Fifty-seven horses had abnormal findings on cervical vertebral radiographs, and 14 had myelographic findings consistent with compressive myelopathy. No antemortem diagnostic test results were consistently associated with necropsy diagnosis of neurodegenerative disease. All 100 horses had degenerative lesions characteristic of eNAD in the brainstem gray matter, and 24 had concurrent degenerative features of EDM in the spinal cord white matter. CONCLUSIONS AND CLINICAL IMPORTANCE: Clinical and histopathologic findings in this large group of horses with neurodegenerative disease were most consistent with eNAD/EDM, but with a different signalment and clinical presentation from earlier descriptions. The increasing occurrence of neurodegenerative disease in horses and the safety risk posed emphasize the importance of focused research in affected horses.

Genetic polymorphisms in vitamin E transport genes as determinants for risk of equine neuroaxonal dystrophy.

BACKGROUND: Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy (eNAD/EDM) is an inherited neurodegenerative disorder associated with vitamin E deficiency. In humans, polymorphisms in genes involved in vitamin E uptake and distribution determines individual vitamin E requirements. HYPOTHESIS/OBJECTIVES: Genetic polymorphisms in genes involved in vitamin E metabolism would be associated with an increased risk of eNAD/EDM in Quarter Horses (QHs). ANIMALS: Whole-genome sequencing: eNAD/EDM affected (n = 9, postmortem [PM]-confirmed) and control (n = 32) QHs. VALIDATION: eNAD/EDM affected (n = 39, 23-PM confirmed) and control (n = 68, 7-PM confirmed) QHs. Allele frequency (AF): Publicly available data from 504 horses across 47 breeds. METHODS: Retrospective, case control study. Whole-genome sequencing was performed and genetic variants identified within 28 vitamin E candidate genes. These variants were subsequently genotyped in the validation cohort. RESULTS: Thirty-nine confirmed variants in 15 vitamin E candidate genes were significantly associated with eNAD/EDM (P < .01). In the validation cohort, 2 intronic CD36 variants (chr4:726485 and chr4:731082) were significantly associated with eNAD/EDM in clinical (P = 2.78 × 10-4 and P = 4 × 10-4 , respectively) and PM-confirmed cases (P = 6.32 × 10-6 and 1.04 × 10-5 , respectively). Despite the significant association, variant AFs were low in the postmortem-confirmed eNAD/EDM cases (0.22-0.26). In publicly available equine genomes, AFs ranged from 0.06 to 0.1. CONCLUSIONS AND CLINICAL IMPORTANCE: Many PM-confirmed cases of eNAD/EDM were wild-type for the 2 intronic CD36 SNPs, suggesting either a false positive association or genetic heterogeneity of eNAD/EDM within the QH breed.

Generalized myokymia, or neuromyotonia, or both in dogs with or without spinocerebellar ataxia.

BACKGROUND: KCNJ10 and CAPN1 variants cause "spinocerebellar" ataxia in dogs, but their association with generalized myokymia and neuromyotonia remains unclear. OBJECTIVE: To investigate the association between KCNJ10 and CAPN1 and myokymia or neuromyotonia, with or without concurrent spinocerebellar ataxia. ANIMALS: Thirty-three client-owned dogs with spinocerebellar ataxia, myokymia neuromytonia, or a combination of these signs. METHODS: Genetic analysis of a cohort of dogs clinically diagnosed with spinocerebellar ataxia, myokymia or neuromyotonia. KCNJ10 c.627C>G and CAPN1 c.344G>A variants and the coding sequence of KCNA1, KCNA2, KCNA6, KCNJ10 and HINT1 were sequenced using DNA extracted from blood samples. RESULTS: Twenty-four Jack Russell terriers, 1 Jack Russell terrier cross, 1 Dachshund and 1 mixed breed with spinocerebellar ataxia were biallelic (homozygous) for the KCNJ10 c.627C>G variant. Twenty-one of those dogs had myokymia, neuromyotonia, or both. One Parson Russell terrier with spinocerebellar ataxia alone was biallelic for the CAPN1 c.344G>A variant. Neither variant was found in 1 Jack Russell terrier with ataxia alone, nor in 3 Jack Russell terriers and 1 Yorkshire terrier with myokymia and neuromyotonia alone. No other causal variants were found in the coding sequence of the investigated candidate genes in these latter 5 dogs. CONCLUSION: The KCNJ10 c.627C>G variant, or rarely the CAPN1 c.344G>A variant, was confirmed to be the causal variant of spinocerebellar ataxia. We also report the presence of the KCNJ10 c.627C>G variant in the Dachshund breed. In dogs with myokymia and neuromyotonia alone the reported gene variants were not found. Other genetic or immune-mediated causes should be investigated to explain the clinical signs of these cases.

Dystonic head tremor in paroxysmal dyskinesia in 17 dogs (2021-2023).

BACKGROUND: Dystonia is a common component of the movement disorder paroxysmal dyskinesia (PD) in dogs. However, the incidence of dystonic head tremor (DHT) in these dogs has not previously been evaluated. METHODS: The medical records of dogs presenting with PD between 2021 and 2023 were retrospectively reviewed, and those with available video footage and the presence of a head tremor were selected for further analysis. RESULTS: Seventeen of the 39 (43.6%) dogs diagnosed with PD that had video footage available manifested DHT. Poodle or Poodle-cross was the most commonly affected breed (7/17). DHTs were described as fine irregular head tremors accompanied by cervical dystonia (17/17), truncal (11/17) or head (10/17) sway, shifting limb (10/17) or single limb (6/17) dystonia, freezing (8/17), ataxia (6/17), ptyalism (5/17), falling (5/17), kyphosis (4/17) and prayer posture (4/17). Neurological examination and advanced imaging, when available, were within normal limits. LIMITATIONS: The limitations of the study include its retrospective nature, the lack of video recordings for all PD patients and the lack of electrophysiological evaluation of tremors and electroencephalography. CONCLUSIONS: DHT exists in dogs with PD; it has characteristic features, and it should be considered in differential diagnoses for dogs with head tremors.

A novel surgical technique for treatment of cervical vertebral stenotic myelopathy (wobbler syndrome) in a filly.

Cervical vertebral stenotic myelopathy (CVSM), also known as equine wobbler syndrome or cervical ataxia, is a devastating neurological syndrome resulting from compression of the spinal cord at the cervical region. This report describes a novel surgical technique for treatment of 16-month-old Arabian filly with CVSM. The filly showed grade 4 ataxia, hypermetria, weakness of the hind limbs, stumbling during walking, and abnormal gait. Case history, clinical signs and myelography revealed spinal cord compression between the C3 and C4 and C4-C5. The filly underwent a novel surgical interference for decompression and stabilization of the point of stenosis using specially designed titanium plate and intervertebral spacer. Evidence of arthrodesis with absence of complications was confirmed by periodic radiography over eight months of postoperative care. The new technique applied in this cervical surgery was efficient for the decompression and stabilization of the vertebrae, allowing arthrodesis development and remission of the clinical signs. The obtained results encourage further assessment of this novel procedure in horses clinically affected by CVSM.

Cerebrospinal fluid and serum proteomic profiles accurately distinguish neuroaxonal dystrophy from cervical vertebral compressive myelopathy in horses.

BACKGROUND: Cervical vertebral compressive myelopathy (CVCM) and equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM) are leading causes of spinal ataxia in horses. The conditions can be difficult to differentiate, and there is currently no diagnostic modality that offers a definitive antemortem diagnosis. OBJECTIVE: Evaluate novel proteomic techniques and machine learning algorithms to predict biomarkers that can aid in the antemortem diagnosis of noninfectious spinal ataxia in horses. ANIMALS: Banked serum and cerebrospinal fluid (CSF) samples from necropsy-confirmed adult eNAD/EDM (n = 47) and CVCM (n = 25) horses and neurologically normal adult horses (n = 45). METHODS: . A subset of serum and CSF samples from eNAD/EDM (n = 5) and normal (n = 5) horses was used to evaluate the proximity extension assay (PEA). All samples were assayed by PEA for 368 neurologically relevant proteins. Data were analyzed using machine learning algorithms to define potential diagnostic biomarkers. RESULTS: Of the 368 proteins, 84 were detected in CSF and 146 in serum. Eighteen of 84 proteins in CSF and 30/146 in serum were differentially abundant among the 3 groups, after correction for multiple testing. Modeling indicated that a 2-protein test using CSF had the highest accuracy for discriminating among all 3 groups. Cerebrospinal fluid R-spondin 1 (RSPO1) and neurofilament-light (NEFL), in parallel, predicted normal horses with an accuracy of 87.18%, CVCM with 84.62%, and eNAD/EDM with 73.5%. MAIN LIMITATIONS: Cross-species platform. Uneven sample size. CONCLUSIONS AND CLINICAL IMPORTANCE: Proximity extension assay technology allows for rapid screening of equine biologic matrices for potential protein biomarkers. Machine learning analysis allows for unbiased selection of highly accurate biomarkers from high-dimensional data.

Otitis media with effusion in two Boston terrier dogs.

Otitis media (OM) in dogs can occur as a primary condition instead of as an extension of an otitis externa (OE), characterized by the presence of fluid in the middle ear (ME) referred to as OM with effusion (OME). OME has been reported in a brachycephalic breed (boxer), and the same condition is described as primary secretory OM in Cavalier King Charles Spaniels. These dogs can be asymptomatic or present with pain, facial nerve paralysis and reduced hearing. This report describes two cases of OME with associated neurologic signs in Boston terriers with no previous history of OE, normal external ear canals and tympanic membranes. Neurologic evaluation revealed right head tilt along with vestibular ataxia and frequent walking tight circles to the right in case 1, and a dull mentation with a right-sided head tilt and torticollis, vestibular tetra-ataxia, ambulatory tetraparesis and circling to the right in case 2. MRI imaging of the brain was performed. Results showed bilateral OM with right-sided otitis interna and equivocal associated otogenic meningitis in case 1 and right-sided OM in case 2. Myringotomy was performed, and both dogs' ME sampled for cytology that only revealed inflammatory cells; and bacterial cultures which revealed a light growth of Pseudomonas aeruginosa in case 1. ME were flushed with sterile saline. Oral glucocorticoids and antibiotics based on the susceptibility results, and a compound antibiotic and glucocorticoid ear solution were prescribed to case 1. Neurologic improvement was observed a few days after the appointment, but a mild right-sided head tilt remained evident. Owner of case two elected humane euthanasia due to patient respiratory difficulties upon anaesthetic recovery and other concurrent healthy concerns. Current findings reinforce that brachycephalic dogs may be prone to develop OME, and advanced imaging tests are key to the diagnosis.

Intracranial medulloblastoma as the cause of progressive ataxia in a 6-month-old draft horse cross gelding.

We describe the unique clinical presentation of a central nervous system neoplasm in a 6-month-old draft horse cross gelding. Based on the neurologic examination at admission, neurolocalization was most consistent with a mildly asymmetric cervical, multifocal, or diffuse myelopathy. Mild vestibular involvement also was considered, but no cranial nerve deficits were observed. The gelding was negative for Sarcocystis neurona or Neospora hughesi based on paired serum and cerebrospinal fluid (CSF) samples analyzed, with no evidence of cervical compression based on contrast myelography. The horse was euthanized because of progression of clinical signs. At necropsy, a mass was identified associated with the cerebellum, and histopathology was consistent with medulloblastoma, which has not been reported previously in the horse.

Cerebellar abiotrophy in an Icelandic horse.

BACKGROUND: Cerebellar abiotrophy (CA) is an uncommon hereditary neurodegenerative disorder affecting the cerebellar Purkinje cells. Equine CA has been reported in several breeds, but a genetic etiology has only been confirmed in the Arabian breed, where CA is caused by an autosomal recessive mutation. CASE PRESENTATION: Clinical and histological findings consistent with CA are reported in an 8.5-month-old Icelandic filly. The filly showed a perceived sudden onset of marked head tremor, incoordination, ataxia, lack of menace response and a broad-based stance. Cerebrospinal fluid, hematological and biochemical findings were all within the normal range, ruling out several differential diagnoses. Post mortem histopathological examination revealed Purkinje cell degeneration accompanied by astrogliosis. Assessment of the filly's pedigree revealed that its parents shared a common ancestor. CONCLUSIONS: To the authors' knowledge, this is the first report of CA in the Icelandic breed. The identification of a common parental ancestor makes autosomal recessive inheritance of CA in this filly possible, but this would need to be confirmed by further studies. Veterinarians and breeders working with Icelandic horses should be aware of this condition and report suspected cases in order to support genetic investigation.

Rehabilitation: Proprioception, Incoordination, and Paresis.

Physiotherapeutic exercises aimed at stimulating motor control, flexibility, and stability are regularly employed in human physical therapy programs. Specifically, the use of such exercises has been shown to reduce both pain and reinjury. Pursuant to the equine patient, several core strengthening exercises and their role in activating deep epaxial musculature to subsequently improve postural motor control and alter thoracolumbar kinematics have been investigated. Both baited and passive exercises offer opportunities to facilitate stretching during dynamic phases and strengthening during static phases of exercise. Blanket recommendations regarding prescription of exercises is not advised, individual patient prescription should be considered in context of handler safety, specific rehabilitation goals, and patient ability to effectively complete the exercise.

Epidemiological investigation of equine hindlimb ataxia with Setaria digitata in South Korea.

BACKGROUND: Since 2013, the number of requests for diagnosis for horses based on neurological symptoms has increased rapidly in South Korea. The affected horses have commonly exhibited symptoms of acute seasonal hindlimb ataxia. A previous study from 2015-2016 identified Setaria digitata as the causative agent. OBJECTIVES: This study is an epidemiological investigation to find out risk factors related to the rapid increase in hindlimb ataxia of horses due to aberrant parasites in South Korea. METHODS: An epidemiological investigation was conducted on 155 cohabiting horses in 41 horse ranches where the disease occurred. The surrounding environment was investigated at the disease-causing horse ranches (n = 41) and 20, randomly selected, non-infected ranches. RESULTS: Hindlimb ataxia was confirmed in nine cohabiting horses; this was presumed to be caused by ectopic parasitism. Environments that mosquitoes inhabit, such as paddy fields within 2 km and less than 0.5 km from a river, had the greatest association with disease occurrence. CONCLUSIONS: Most horse ranches in South Korea are situated in favorable environments for mosquitoes. Moreover, the number of mosquitoes in the country has increased since 2013 due to climate change. Additional research is required; however, these data show that it is necessary to establish guidelines for the use of anthelmintic agents based on local factors in South Korea and disinfection of the environment to prevent disease outbreaks.

Cholesterol granuloma associated with degenerative neuropathy in the cauda equina of a dog.

An 8-y-old Labrador Retriever dog had mild ataxia of the hindlimbs 4 mo after lumbosacral dorsal laminectomy for intervertebral disk disease. Ataxia of the hindlimbs gradually worsened over the next 6 y. On autopsy, gross lesions were not recognized in the spinal cord. Histopathology revealed an intradural extraparenchymal cholesterol granuloma in the cauda equina associated with remnant nerve roots. Nerves associated with the cholesterol granuloma had axonal degeneration, myelin vacuolation, and edema. In those foci, macrophages were increased in number between nerve fibers. Immunohistochemistry for neurofilament protein and Luxol fast blue staining highlighted the presence of remnant axons and myelin sheaths within the granuloma. Inflammatory cell infiltrates in the granuloma were mainly macrophages and CD3- or CD20-immunopositive T or B lymphocytes, respectively. We conclude that the cholesterol granuloma likely formed subsequent to degenerative neuropathy in the cauda equina.